6. Chung P, Hermann L. Acute Decompensated Heart Failure: Formulating an Evidence Based Approach to Diagnosis and treatment. Mt. Sinai J of Med 2006;73(2): 506-27.
7. Chung P, Hermann L. Acute Decompensated Heart Failure: Formulating an Evidence Based Approach to Diagnosis and treatment. Mt. Sinai J of Med 2006;73(2): 506-27.
8.
9.
10.
11.
12.
13.
14. A QRS duration of >0.1, >0.11 or >0.12 s was
highly specific (63, 90 and 98%) but less sensitive
(84, 81 and 75%) for the prediction of LVSD
15.
16.
17.
18.
19. BNP
NT pro-BNP
Age
All
< 50
50-70
> 70
Rule Out
< 100+
< 300*
< 300*
< 1200₸
Sens/Spec
90%/74%
99%/85%
99%/85%
97%/55%
Rule In
> 400+
>450*
>900*
>4500₸
Sens/Spec
81%/90%
93%/95%
91%/80%
64%/86%
*Januzzi, Jr. et al Am J Cardiol 2005 ₸Berdague et al. Am Heart J 2006 +Korenstein BMC Emerg Med 2007
20.
21.
22.
23.
24.
25.
26.
27.
28. Acute vs Chronic
High-Output vs Low-Output
Right vs Left
Systolic vs Diastolic
Dilated vs Hypertrophic vs Restrictive
39. What infusion rate of nitroglycerin is appropriate for this patient?
A.Start at 5 mcg/min and titrate up
B.Start at 100 mcg/min and titrate down
C.Start at 100 mcg/min and titrate up
D.Give 1 SL NTG q 5 min
E.Apply 0.5 inch of nitro paste and cross fingers
40. Nitroglycerin is an oily liquid that may explode when subjected to heat, shock or flame. It is dangerously sensitive and dropping or bumping a container may cause it to explode.
–Wikipedia
44. •Preload/Afterload Reduction
•Captopril SL resulted in more rapid clinical improvement when added to standard regimen over placebo*
•Enalaprilat IV is well tolerated, and reduces PCWP**
•Should be started within 24 hours***
*Hamilton R. Acad Emerg Med 1996.
**Annane D. Circulation 1996.
***Buccelletti F. Mt Sinai J of Med 2006.
51. •NIPPV
•High dose NTG ggt for hypertensive
–Start @ 100 mcg/min
•NE and/or Dobutamine for hypotensive
•Just say no to furosemide
Editor's Notes
I also submit to you that you can turn this pt around in 30 minutes, and spare them the laryngoscope. Isn’t this why we do Emergency Medicine? To fix someone.
Two patients: one acute, one chronic. I submit to you that management of the chronic CHF pt is boring, and will not be covered here.
The acute one is obvious because no one is diaphoretic for one month before calling 9-1-1.
Cardiorenal Model: 1940s model. Ventricular dysfunction decreased renal perfusion edema. Goal was to increase renal perfusion with diuretics, which is largely how most practice today. Doesn’t explain progressive nature, and doesn’t explain vasoconstriction which contributes to decreased cardiac performance
Cardiocirculatory Model: 1970s model. Vasoconstriction heart failure. Goal was to vasodilate to improve cardiac function. Still doesn’t explain progressive nature of dz.
Neurohormonal Model: 1990s model. Neurohormones have effects on cardiac performance, vascular tone, and intravascular volume.
Cardiorenal Model: 1940s model. Ventricular dysfuntion decreased renal perfusion edema. Goal was to increase renal perfusion with diuretics, which is largely how most practice today. Doesn’t explain progressive nature, and doesn’t explain vasoconstriction which contributes to decreased cardiac performance
Cardiocirculatory Model: 1970s model. Vasoconstriction heart failure. Goal was to vasodilate to improve cardiac function. Still doesn’t explain progressive nature of dz.
Neurohormonal Model: 1990s model. Neurohormones have effects on cardiac performance, vascular tone, and intravascular volume.
JVD
Pitting Edema
128 consecutive patients with suspected cardiac disease, 66 with confirmed LVEF<50%
Cardiomegaly, fluid in the middle fissure, cephalization, kerly b lines, increased interstitial markings
880 ED pts with acute dyspnea, 447 with acute heart failure as determined by two cardiologists retrospectively
Back to our case: NT-proBNP 1574, afib RVR VR 122
Why do I say no if diuresis is the most commonly accepted goal of initial therapy?
Remember, the primary insult is reduced LV contractility, and therapy should be aimed at improving contractility and, thereby, improving CO.
Of 120 patients admitted for HF, 54% had <2 lbs weight gain, suggesting most patients with AHF are not volume overloaded
3 Groups with at least 10 each, in ICU setting, all with Swan-Ganz catheter. None had received furosemide prior to initiating study.
Initial increase in PCWP (although small) in Groups 1 & 2, decrease only in Group that had already been pre/afterload reduced.
So what? What about patient outcomes?
All pts initially treated with oxygen 10 L/min, intravenous furosemide 40 mg, and morphine 3 mg bolus.
Group A received isosorbide dinitrate (3 mg bolus administered intravenously every 5 min; n=56) – equivalent to 600 mcg/min
Group B received furosemide (80 mg bolus administered intravenously every 15 min, as well as isosorbide dinitrate 1 mg/h, increased every 10 min by 1 mg/h
Objective scoring system: Objective response was determined by a scoring system based on changes in respiratory rate, heart rate, blood pressure, rales, respiratory distress, and mental status.
Group A: NTG and furosemide, Group B: MS and furosemide, Group C: NTG furosemide and MS, Group D: NTG and furosemide
Just a reminder that exploding your patients with NTG is generally considered poor form
How high is too high?
One patient received nine 2 mg boluses q 3min, an equivalent infusion of 700 mcg/min
Less bipap, intubations, and ICU admissions than historical controls
Study basically states that extremely high-dose NTG is safe
*If normotensive, a single 12.5 mg tab was given SL, if hypertensive two tabs were given
The history of Nesiritide is an interesting one. Approved for use by FDA in 2001, it is a recombinant BNP. It was approved for use based on studies that showed a decreased in PCWP in the 90s. Subsequently, a JAMA meta-analysis in 2005 suggested worse mortality, and it fell out of favor. The ASCEND-HF trial ended the controversy.
